Expression and prognostic value of hsa-miR-206 in non-triple-negative breast cancer

Abstract Objective This study aims to analyze the expression and prognostic value of hsa-miR-206 in non-triple-negative breast cancer. Methods The expression of has-miR-206 in breast cancer and normal breast tissues was analyzed using the dbDEMC 2.0 database. The TCGA dataset was used to verify hsa-miR-206 expression and analyze its role in breast cancer pathways. In situ hybridization was conducted on tissue microarrays comprising 80 breast cancer specimens and corresponding paracancerous tissues. The relationship between hsa-miR-206 expression and the clinicopathological features of patients with non-triple-negative breast cancer was assessed. Patients were divided into high and low-expression groups based on hsa-miR-206 expression levels, and survival curves were plotted. Online TCGA data analysis was performed to determine intersecting genes and action pathways of hsa-miR-206, with further STRING network analysis to explore possible mechanisms involving hsa-miR-206-related intersecting genes. Results The dbDEMC 2.0 and TCGA database and in situ hybridization assay confirmed significantly lower hsa-miR-206 expression in breast cancer tissues compared to paracancerous tissues. In the luminal A subtype, hsa-miR-206 expression was markedly lower in ER-positive human breast cancer tissues than in paracancerous tissues. In the HER2+ subtype, the positive expression rate of hsa-miR-206 in cancerous tissues was 28%, while that in paracancerous tissues was 72%. Patients under 50 years old showed significantly lower positive expression rates. Additionally, hsa-miR-206 expression level correlated significantly with histological grade and Ki-67 expression but not with tumor size or sex hormone receptor status. Kaplan–Meier Plotter analysis of the TCGA and METABRIC databases indicated that patients with low hsa-miR-206 expression had longer overall survival (OS). Subtype-specific analysis showed varying OS benefits: longer OS in luminal A and B breast cancer with low hsa-miR-206 and a slight increase in OS in HER2+ breast cancer. Target genes regulated by hsa-miR-206 were linked to cell cycle and estrogen signaling pathways. Conclusion Downregulation of hsa-miR-206 expression in breast cancer may prolong patient OS. Hsa-miR-206 plays distinct roles across breast cancer subtypes, potentially through different target genes affecting cell cycle and estrogen signaling, which underscore its prognostic implications.